Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury

Abstract

Cardiac arrest (CA) is a well-known cause of global brain ischemia. After CA and subsequent loss of consciousness, oxygen tension starts to decline and leads to a series of cellular changes that will lead to cellular death, if not reversed immediately, with brain edema as a result. The electroencephalographic activity starts to change as well. Although increased intracranial pressure (ICP) is not a direct result of cardiac arrest, it can still occur due to hypoxic-ischemic encephalopathy induced changes in brain tissue, and is a measure of brain edema after CA and ischemic brain injury. In this review, we will discuss the pathophysiology of brain edema after CA, some available techniques, and methods to monitor brain oxygen, electroencephalography (EEG), ICP (intracranial pressure), and microdialysis on its measurement of cerebral metabolism and its usefulness both in clinical practice and possible basic science research in development. With this review, we hope to gain knowledge of the more personalized information about patient status and specifics of their brain injury, and thus facilitating the physicians' decision making in terms of which treatments to pursue.

Keywords: Electrophysiologic monitoring; ICP monitoring; brain injury after cardiac arrest; brain oxygen monitoring; cerebral autoregulation; intracranial pressure; metabolic tracing and cardiac arrest brain injury; microdialysis.

Figure 1

Demonstrates the cascade of effects after cardiac arrest and decreased oxygen tension has on the brain cellular function due to decreased ATP (Adenosine triphosphate), increased excitatory amino acids, and the failure of Calcium efflux pump to work. ICP (intracerebral Pressure), ROS (reactive oxygen species), RNS (reactive nitrogen species). The thin arrows indicate the increase or decrease of either a substance or diagrams the consequences of cardiac arrest.

Figure 2

Cardiac arrest and the resulting activation of the inflammatory cascade is demonstrated on the figure above. Inflammation is depicted as a factor that contributes to secondary neuronal injury and death. The dashed line represents a division of the brain and periphery. This figure shows the migration of cells from the blood into the brain. The arrows in green demonstrate the factors that will lead to Secondary Neuronal Injury and Neuronal Death. Penetration of Microglia in the brain also leads to stimulation of Cytokines, inflammation, and ROS (reactive oxygen species). The upward facing arrows indicate the increase in a certain factor or cell after cardiac arrest. Gerry Shaw, Microglia and neurons, 25 July 2005 by creative commons; Hematologist, Segmented Neutrophils, 31 August 2009, Creative Commons.

Figure 3

Figure demonstrating the result of decreased brain oxygen and consequent lactate production. A microdialysis probe detects biomarkers, such as Lactate/Pyruvate ratio (LP) that will indicate ischemia or mitochondrial dysfunction.